Abstract

Background Mentalising impairment (an impaired ability to think
about people in terms of their mental states) has frequently been associated
with schizophrenia.

Aims To assess the magnitude of the deficit and analyse associated
factors.

Method Twenty-nine studies of mentalising in schizophrenia (combined
n=1518), published between January 1993 and May 2006, were included
to estimate overall effect size. Study descriptors predicted to influence
effect size were analysed using weighted regression-analysis techniques.
Separate analyses were performed for symptom subgroups and task types.

Results The estimated overall effect size was large and
statistically significant (d=–1.255, P<0.0001) and
was not significantly affected by sample characteristics. All symptom
subgroups showed significant mentalising impairment, but participants with
symptoms of disorganisation were significantly more impaired than the other
subgroups (P<0.01).

Conclusions This meta-analysis showed significant and stable
mentalising impairment in schizophrenia. The finding that patients in
remission are also impaired favours the notion that mentalising impairment
represents a possible trait marker of schizophrenia.

`Theory of mind' and `mentalising' refer to the cognitive ability to
attribute mental states such as thoughts, beliefs and intentions to people,
allowing an individual to explain, manipulate and predict behaviour. In 1992
Frith proposed a relationship between theory of mind and schizophrenia, and
argued that several symptoms of schizophrenia could be explained by
mentalising impairment (Frith,
1992). This led to a substantial body of research which has
recently been critically reviewed twice
(Brüne, 2005a;
Harrington et al,
2005a). In both reviews it was concluded that theory of
mind is impaired in individuals with schizophrenia. Although these reviews
were executed thoroughly, they are limited to a qualitative description of the
observed deficit, thus lacking important information on the magnitude of the
effect. The purpose of this meta-analysis is to produce a synthesised effect
size estimate that has considerably more power than the individual studies. In
addition, effects of study characteristics on the findings are analysed.

METHOD

Study selection

An extensive literature search was conducted in the electronic databases
Medline, EMBASE and PsycINFO (January 1993 to May 2006) using the following
key words: theory of mind, mentalizing, social cognition, schizophrenia, and
psychosis. Additional studies were identified by checking the reference lists
from identified reviews and papers on the topic. To ensure that we did not
overlook studies published by May 2006 but not included in the computerised
databases by that date, a journal-by-journal search was performed in the
January 2006 to May 2006 editions of the American Journal of Psychiatry,
Biological Psychiatry, Journal of Nervous and Mental Disease, Psychiatry
Research, Schizophrenia Bulletin, Schizophrenia Research and
Psychological Medicine. Studies considered eligible for this
meta-analysis were empirical research studies written in the English language
and published in peer-reviewed journals. Research samples had to be composed
of adults diagnosed with schizophrenia or schizoaffective disorder according
to the established diagnostic systems (DSM or ICD). Their sample group's
mentalising performance had to be compared with that of healthy controls.
Measures of mentalising included in this meta-analysis are described below.
Finally, sufficient data had to be reported for the computation of the
standardised mean difference (Lipsey &
Wilson, 2001).

Types of mentalising tasks

There is a fair amount of agreement on the definition of theory of mind
among researchers. However, this definition is broad, perhaps reflecting the
fact that it is probably not a unitary function. This has led to a wide
variation in the operationalisation of the concept. One of the most frequently
used types of mentalising tasks is the false belief or deception task (e.g.
Frith & Corcoran, 1996;
Corcoran et al, 1997;
Doody et al, 1998;
Mazza et al, 2001).
In a first-order false belief/deception task, the ability to understand that
someone can hold a belief that is different from the actual state of affairs
is assessed. In a second-order false belief/deception task, participants have
to infer the (false) beliefs of one character about the (false) beliefs of a
second character.

A second type of theory of mind task commonly used in schizophrenia
research is an intention-inferencing task, in which the ability to infer a
character's intentions from information in a short story is assessed (e.g.
Sarfati et al,
1997a,b,
1999,
2000;
Sarfati & Hardy-Baylé,
1999). A third type of task measures the ability to understand
indirect speech, such as in irony, banter, hints and metaphors (e.g.
Corcoran et al, 1995;
Langdon et al, 2002; Corcoran,
2003; Corcoran & Frith,
2003; Craig et al,
2004). This is based on the notion that for the understanding of
indirect speech an understanding of another person's mental state is required
(e.g. Sperber & Wilson,
2002). However, Langdon & Coltheart
(2004) showed that
comprehension of irony and comprehension of metaphors are unrelated and that
having an intact theory of mind is a prerequisite for the interpretation of
irony but not for the interpretation of metaphors. Therefore, data on the
interpretation of metaphors were excluded from this meta-analysis.

A fourth, less commonly used type of theory of mind task in schizophrenia
research is the attribution of mental states to animated geometric shapes
which interact in a `socially' complex way
(Blakemore et al,
2003; Russell et al,
2006). This type of task may not be fully comparable with the
other theory of mind tasks because of the higher level of abstraction
involved. Finally, in some studies the `eyes' task is used, in which
participants have to infer mental states from looking at pictures of eyes
(Kington et al, 2000;
Russell et al, 2000;
Kelemen et al, 2005).
This has been referred to as a theory of mind task, but at face value the
construct being measured seems to be different from that assessed by the other
paradigms, perhaps assessing emotion recognition abilities or empathy rather
than theory of mind.

Since there is a serious lack of research on the psychometric properties
(including construct validity and criterion validity) of the many different
theory of mind tasks that have been developed
(Harrington et al,
2005a), it may not be possible to formulate completely
objective inclusion criteria regarding the type of tasks used in the studies.
In this meta-analysis this problem is addressed statistically in two ways.
First, homogeneity analyses are used to check whether the grouping of effect
sizes from different studies shows more variation than would be expected from
sampling error alone, indicating that the effect sizes may not be comparable.
A second approach to this problem is to break down the overall mean effect
size into mean effect sizes for different types of tasks. For these mean
effect sizes per type of task to be meaningful, we (subjectively) set a
minimum of five eligible studies per sub-task analysis. This led to the
exclusion of two studies using tasks assessing the attribution of mental
states to abstract shapes rather than humans
(Blakemore et al,
2003; Russell et al,
2006), and three studies in which the `eyes' task was used
(Kington et al, 2000;
Russell et al, 2000;
Kelemen et al,
2005).

Schizophrenia subgrouping

Ever since Frith's first proposal
(Frith, 1992), the association
between mentalising and the core symptoms of schizophrenia has been an
important focus of research interest. Schizophrenia is a heterogeneous
disorder and various subgrouping methods have been used, based on different
theories regarding the relationship between mentalising and
symptomatology.

In earlier studies, Frith and colleagues divided their schizophrenia
samples into six symptom subgroups
(Corcoran et al,
1995). In their later studies, the number of subgroups was reduced
to four, categorised as follows:

The first group was predicted to be the most impaired, because of these
patients' incapacity to represent the mental states of others as well as
themselves. Paranoid patients would perform poorly because of their
difficulties in monitoring other people's intentions. Patients whose symptoms
were in remission and patients with passivity symptoms were predicted to have
normal mentalizing abilities. These hypotheses were largely confirmed and have
repeatedly been replicated (Frith &
Corcoran, 1996; Corcoran
et al, 1997; Pickup & Frith, 2001).

Sarfati and colleagues (Sarfati et al,
1997a,b,
1999;
Sarfati & Hardy-Baylé,
1999) and Zalla et al
(2006) suggested that
impairment of theory of mind is related to thought disorder, reflecting an
executive functioning deficit. Thus, their samples were divided into those
with and those without thought disorder. In all of their studies
thought-disordered participants performed significantly more poorly than
healthy controls. However, in two of the studies the non-disorganised
participants also showed poor performance
(Sarfati et al,
1997b; Zalla et
al, 2006).

Three research groups studied the relationship between mentalising and
paranoid delusions (Randall et
al, 2003; Craig et
al, 2004; Harrington
et al, 2005b). In all three studies patients
with paranoid delusions showed impairment of theory of mind relative to the
normal control group. However, in the study by Randall et al
(2003), theory of mind
performances of the paranoid and non-paranoid subgroups did not differ
significantly from each other. Lastly, Herold et al
(2002) investigated whether
the deficit in theory of mind was state- or trait-dependent and therefore
assessed patients whose schizophrenia was in remission. Results showed that
theory of mind impairment was still present in the remission phase of the
illness.

Moderator variables

Published research suggests a number of variables that may affect
mentalising performance and thus influence effect size. Hence, we aimed to
code these variables in order to evaluate their influence on the effect size.
Potential moderator variables at individual patient level are age, gender,
medication, IQ, disease status (acute, chronic or in remission), severity of
psychopathology, and symptoms. To analyse the effect of specific clusters of
symptoms on mentalising impairment, the symptom subgroups used by different
research groups were divided into four categories:

Potential moderators at study level are the matching of patients and
controls on group characteristics (e.g. mean age, mean IQ, gender
distribution), type of mentalising task used, and whether the task is
administered verbally or non-verbally. Four types of theory of mind tasks were
distinguished: first-order false belief/deception; second-order false
belief/deception; intention inferencing; and comprehension of indirect speech.
Some tasks did not fit in any of these categories, for example the false
belief/deception tasks for which the orders were unknown or mixed.

Within the different task paradigms there is also variation in whether
tasks are presented in a verbal or non-verbal form. It has been suggested that
verbalisation may be impoverished in schizophrenia and may constitute an
experimental bias in favour of a theory of mind deficit in people with
schizophrenia (e.g. Sarfati et
al, 1999). In a separate coding, tasks were classified as
verbal or non-verbal.

Coding

Each study was coded independently by two authors (M.S. and E.V.). In case
of discrepancies, consensus was reached in conference with the whole research
group. When results were reported in graphical form only an email was sent to
the author with a request for the exact numerical results.

Data collection and analysis

For each study an unbiased standardised mean difference (d), was
calculated using reported means and standard deviations. This effect size
statistic is computed as the difference between the mean of the schizophrenia
group and the mean of the control group, divided by the pooled standard
deviation. Hedges' formula was applied to correct for upwardly biased
estimation of the effect size in small samples
(Lipsey & Wilson,
2001).

When means and standard deviations were not available, d was
calculated from the reported t or F values. In cases where
the only reported outcome variable was the proportion of participants with a
good (or poor) performance, d was estimated using the probit
transformation method (Lipsey &
Wilson, 2001). A sensitivity analysis was performed to check
whether there was any significant effect of using probit-transformed effect
sizes on the overall effect size. In studies in which data were reported for
(symptom) subgroups only, data were first pooled and then compared as one
group with the control group. In addition, the effect sizes of symptom
subgroups were calculated for subsequent analyses. Several studies used more
than one (sub)task to assess theory of mind, and therefore had more than one
effect size; in these cases a pooled effect size was computed. However, if the
authors had included a composite score, the effect size of this score was
calculated. Again, effect sizes for different task types were calculated for
subsequent analyses. In addition to the individual effect sizes and 95%
confidence intervals, P values were calculated for each study using
two-tailed independent t-tests and χ2-tests.

The mean effect size across studies was calculated by weighting each effect
size by the inverse of its sampling variance. A confidence interval and
z-value were calculated to examine the statistical significance of
the effect. To test whether the individual effect sizes are good estimators of
the population effect size, the homogeneity statistic Q was
calculated (Lipsey & Wilson,
2001). Because sample sizes are small in the subgroup and task
type analyses (see below), a random effects model was fitted to the data
(Lipsey & Wilson, 2001).
To examine publication bias, a fail-safe number was computed using Orwin's
formula (Lipsey & Wilson,
2001). This indicates the number of studies with null effects that
have to reside in file drawers to reduce the mean effect size to a negligible
level (which we set at 0.2). Weighted regression analysis was performed using
the statistical package Meta-Stat (Rudner
et al, 2002) to evaluate whether group differences in IQ,
gender and age had an impact on effect size. Other variables with a potential
influence on effect size, such as patient status, medication use and severity
of psychopathology, could not be analysed because of the small number of
studies reporting results for these parameters. Separate analyses were
performed to analyse whether mentalising impairment is different for different
symptom subgroups or for different types of mentalising tasks.

RESULTS

The literature search resulted in a total of 32 studies meeting the
inclusion criteria. One publication
(Langdon et al,
2002a) was excluded because data concerning the same
participants had been reported in another paper
(Langdon et al,
2002b). Sample characteristics (n, mean age,
percentage of males, mean score on the Binois–Pichot Vocabulary Scale
and mean score on the non-verbal theory of mind test) were exactly the same in
two studies by Sarfati and colleagues
(Sarfati & Hardy-Baylé,
1999; Sarfati et al,
2000), suggesting that the same patient samples had been used.
Because in the first of these studies the patient sample was divided into
symptom subgroups, but more control participants and an additional theory of
mind task were used in the latter study, instead of selecting one of the two
studies the results of both were combined. Because we were unable to contact
the authors of one study within the time frame of data collection and data
analysis to obtain the exact numerical results which were not reported in the
article, the results of that study could not be included in the meta-analysis
(Frith & Corcoran, 1996).
The characteristics of the remaining 29 studies with a total of 831 patients
(mean age 35.9 years, 70% male, mean IQ 98.7) and 687 controls (mean age 35.2
years, 60% male, mean IQ 105.3) are listed in
Table 1.

Analysis of the total sample

Figure 1 shows the 29
individual effect sizes with their 95% confidence intervals. None of the
confidence intervals includes the value zero, indicating a statistically
significant effect for each study. The weighted mean effect size of the
combined sample is –1.255 (95% CI –1.441 to –1.069) which is
also statistically significant (z=13.25, P<0.0001).
Homogeneity analysis showed that there was homogeneity among studies
(Q=29.13, d.f.=28, P<0.41), and weighted regression
analysis did not show any relationship between effect size and difference
between patient and control groups in IQ (P=0.193), proportion of
males (P=0.115) and age (P=0.147). The fail-safe number was
153, which indicates that 153 unpublished studies are required to reduce the
effect size of the combined findings to a negligible level.

Analyses of the symptom subgroups

Mean effect sizes and confidence intervals of the symptom subgroups are
displayed in Fig. 2. The
disorganised patients performed worst on the mentalising tasks compared with
healthy controls (d=–2.231, 95% CI –2.565 to –
1.897, P<0.01). The confidence interval of the mean effect
size in the disorganized subgroup shows no overlap with that in the
non-disorganised (d=–1.278, 95% CI –1.771 to –
0.785, P<0.01) and paranoid subgroups
(d=–1.241, 95% CI –1.514 to –0.968,
P<0.01), indicating that the difference between the disorganised
subgroup and the other subgroups is statistically significant. This was
confirmed by post hoc comparisons of the mean effect size of the
disorganised subgroup v. the mean effect sizes of the other three
symptom subgroups (all P values <0.01). Interestingly, patients in
remission also showed a significantly worse performance than controls
(d=<0.692, 95% CI –1.017 to –0.367,
P<0.01). The homogeneity statistic of the non-disorganised
subgroup was statistically significant (Q=7.3816, d.f.=4,
P<0.05), indicating that the effect sizes within this subgroup
analysis differed more than would be expected from sampling error alone,
perhaps owing to differences associated with study (or sample)
characteristics. This was somewhat surprising, since four of the five studies
were by the same research group. The finding that the other three homogeneity
statistics were not statistically significant suggests that although different
authors might have used different criteria for their symptom subgroups,
combining these subgroups was meaningful.

Analyses of the types of mentalising tasks

The mean effect sizes and confidence intervals of the four theory of mind
task categories are shown in Fig.
3. The mean effect sizes of the first-order tasks
(d=–1.193, 95% CI –1.666 to –0.720,
P<0.01) and the second-order tasks (d=–1.443, 95%
CI –1.867 to –1.019, P<0.01) have homogeneity
statistics indicating heterogeneity among the effect sizes: Q=97.691,
d.f.=12 (P<0.01) and Q=17.875, d.f.=6
(P<0.01) respectively. In contrast, the mean effect sizes within
both the indirect speech tasks (d=<1.040, 95% CI –1.301 to –
0.779, P<0.01) and the intention-inferencing tasks
(d=–0.959, 95% CI –1.228 to –0.690,
P<0.01) are both homogeneous. The difference between the mean
effect sizes for different subtasks could not be analysed statistically,
because not all effect sizes were statistically independent since in one study
different types of tasks might have been used.

The mean effect size of studies using verbal tasks is comparable with the
mean effect size of studies using non-verbal tasks (verbal,
d=–1.221, 95% CI –1.462 to –0.980; non-verbal
d=–1.251, 95% CI –1.496 to –1.006). The homogeneity
statistics of the verbal and non-verbal tasks both show heterogeneity among
the effect sizes. Again, the difference could not be analysed because of
statistical dependence.

DISCUSSION

The aim of this meta-analysis was to investigate the extent of mentalising
impairment in people with schizophrenia. By combining 29 studies, a total
sample size was created of over 1500 participants. The overall effect size was –
1.1255, indicating that on average the theory of mind performance of
participants with schizophrenia is more than one standard deviation below that
of healthy controls. According to a widely used convention for appraising the
magnitude of effect sizes this is considered a large effect
(Cohen, 1988). Homogeneity
analysis showed that the mean effect size of the combined samples is a good
estimate of the typical effect size in the population. The large fail-safe
number makes the `file drawer' problem, which is a limitation of some
meta-analyses, negligible.

The moderator variables IQ, gender and age did not significantly affect
mean effect size. Thus, the impairment in theory of mind is robust and is not
readily moderated by variables that may seem relevant. However, the effect of
other potentially important moderator variables such as medication use and
duration and severity of illness could not be analysed owing to a lack of
information on these characteristics in many studies.

Participants with schizophrenia who had signs and symptoms of
disorganisation were found to be significantly more impaired in terms of
theory of mind than those in the other symptom subgroups. However, these
results may also be explained by the composition of the disorganised symptom
subgroup. The behavioural subgroup of the studies by Frith and colleagues was
ranked highest in their hierarchical model. Thus, individuals in this group
might also have had symptoms of the paranoid and/or passivity subgroup. This
brings the risk that poorer performance in this group may be explained by
having more severe and complex symptoms
(Harrington et al,
2005a). Similarly, in two of the four studies by Sarfati
and colleagues the disorganised subgroup had more general psychopathology,
which might explain their poorer theory of mind performance
(Sarfati & Hardy-Baylé,
1999; Sarfati et al,
1999).

The mean effect size (d=–0.692) of mentalising impairment in
patients in remission was smaller than in the other symptom subgroups, but is
still considered to be medium to large
(Cohen, 1988). Moreover, this
effect did not differ significantly from the effect sizes of the disorganised
and paranoid subgroups.

Unexpectedly – and despite apparent differences in type and
difficulty of the theory of mind tasks – the mean effect sizes for
different task types were found to be similar. An explanation might be that
our method of grouping studies by task types was not correct. This is
supported by the finding that two of the four task type analyses showed
heterogeneity among effect sizes. However, since there is a lack of research
on the psychometric properties of the tasks that were used, such as construct
and concurrent validity, it is not yet possible to categorise these tasks
objectively.

There was also no difference between the mean effect sizes of verbal and
non-verbal tasks, which is consistent with the findings of Sarfati and
colleagues (Sarfati et al,
1999,
2000). Thus, impairment of
theory of mind does not to appear to be affected by verbalisation deficits
that have been reported in people with schizophrenia.

Mentalising in schizophrenia: generalised v. specific
impairment

As shown by Heinrichs & Zakzanis
(1998), people with
schizophrenia show generalised neurocognitive impairment. On their list of 22
mean effect sizes of common neurocognitive tests, the effect size of
mentalising impairment would be ranked fourth. An interesting question is
whether poor mentalising performance in schizophrenia interacts with or is
influenced by general cognitive impairment. This problem is acknowledged by
some authors, who corrected for general cognitive abilities by matching groups
on IQ, covarying out cognitive variables (e.g. attention, executive
functioning, memory, general picture sequencing abilities) or excluding
participants from statistical analyses if they answered reality questions
about the theory of mind stories incorrectly. In their reviews, Brüne ne
(2005a: p. 25,
Table 1) and Harrington et
al (2005a: pp.
252–267, Table 1)
discussed the empirical evidence as to whether the mentalising deficits in
schizophrenia are specific or the consequence of general cognitive impairment.
In both reviews it was concluded that the evidence speaks in favour of the
notion that there is a specific theory of mind deficit in schizophrenia. As
with many neurocognitive tests, theory of mind tasks probably measure several
component processes at the same time. For example, tasks in which the
comprehension of indirect speech is assessed may require not only mentalising
abilities but also basic language comprehension and expressive language
skills. Possibly, general cognitive abilities represent a necessary but not
sufficient condition for adequate mentalising, which is known as the `building
block' view of social cognition (see Penn
et al, 1997).

Mentalising in schizophrenia: state or trait dependency

In his cognitive model of the relationship between meta-representation and
the signs and symptoms of schizophrenia, Frith assumed that in people with
this disorder, the initial development of mentalising abilities is relatively
normal and that these abilities become impaired as the illness develops
(Frith, 1992). In the
subsequent studies by him and his colleagues, it was predicted and found that
patients who were in remission (i.e. symptom-free) were unimpaired compared
with normal controls (e.g. Corcoran et al,
1995,
1997;
Frith & Corcoran, 1996;
Pickup & Frith, 2001). In
contrast, our meta-analysis has shown that patients have significant
impairment during remission, which is consistent with the findings of Herold
et al (2002). These
findings support the notion that mentalising is not just a consequence of the
acute phase of the disorder but may be trait-dependent. It cannot be excluded
that the criteria for remission (e.g. partial or full remission) used by
Herold et al (2002)
and by Frith and colleagues are different. Other factors such as
(prophylactic) treatment may also explain the divergent findings. However,
more support for the trait argument comes from studies on mentalising in
populations at elevated risk of developing a psychotic illness.

In general, people at genetic risk of schizophrenia show reduced
performance on the more common types of theory of mind tasks
(Wykes et al, 2001;
Irani et al, 2006;
Marjoram et al,
2006), but not on the `eyes' test
(Kelemen et al, 2004;
Irani et al, 2006).
In the study by Schiffman et al
(2004), genetic high-risk
children who would later develop schizophrenia-spectrum disorders had lower
scores on a role-taking task, which the authors considered assessed a facet of
theory of mind. An association between theory of mind performance and
subclinical schizotypal traits has also been found (Langdon & Coltheart,
1999,
2004;
Irani et al, 2006;
Meyer & Shean, 2006).
Pickup (2006) showed that
schizotypal traits analogous to positive symptoms of schizophrenia predicted
poorer mentalising performance, whereas no association was found between
poorer theory of mind and schizotypal traits analogous to the `behavioural
signs' of schizophrenia. Platek et al
(2003) suggested that
contagious yawning is part of a more general phenomenon known as mental state
attribution. Consistent with this hypothesis, susceptibility to contagious
yawning was positively related to performance on (other) mentalising tasks,
and negatively related to schizotypal personality traits. Only in the study by
Jahshan & Sergi (2007) was
there no difference between people with high schizotypy and those with low
schizotypy regarding theory of mind performance. There is thus considerable
evidence that mentalising impairment is a susceptibility indicator for
schizophrenia and hence may be trait-dependent.

Limitations

The first limitation, to which we have already alluded, is that studies
were excluded in which less common types of theory of mind tasks were used.
Because there is no information on the psychometric properties of the many
different tasks, this is somewhat arbitrary. In addition, the categorisation
of task type is not supported by psychometric evidence. Second, the method of
categorising symptom subgroups employed in this meta-analysis should be
considered tentative. The main problem with our approach is that there is
overlap between symptom clusters; for example, the subgrouping method used by
Frith and colleagues is hierarchical, with the behavioural subgroup being the
highest category. This means that patients in that subgroup could also report
paranoid symptoms, but those in the paranoid subgroup could not report
behavioural symptoms. As another example, participants categorised as paranoid
in the study by Harrington et al
(2005b) could also
have formal thought disorder (which was indeed the case). However, in spite of
this limitation, we believe that the results of the subgroup analyses in this
meta-analysis are valuable. This is statistically supported by the homogeneity
analyses, which show that the clustering of symptom subgroups did not result
in more variation than would be expected from sampling error alone and that it
is plausible that the studies within the subgroup analyses are comparable.

Recommendations for future research

The results and limitations of this meta-analysis lead to some
recommendations for future research. First, research focusing on the
mentalising process itself is necessary, addressing questions on what
components it comprises and on how to operationalise them. As has already been
pointed out by Harrington et al
(2005a), it is also
important to establish the psychometric properties of theory of mind tasks.
Second, the finding that the deficit in theory of mind in schizophrenia is
perhaps trait-dependent rather than state-dependent implies that the deficit
may also be present before illness onset. Therefore, there may be a role of
mentalising impairment in the early detection and prediction of schizophrenia,
requiring a longitudinal study examining theory of mind abilities in people at
risk of developing schizophrenia.

Third, the finding that theory of mind impairment may be trait-dependent
also brings to mind a comparison with autism-spectrum disorders. An impaired
ability to understand mental states has been described as one of the core
symptoms of such disorders (Yirmiya et
al, 1998). However, although the risk of psychotic disorder
is elevated in individuals with autism-spectrum disorder
(Stahlberg et al,
2004), most of them will not develop a psychotic disorder. Future
research should focus on what the commonalities and differences are with
regard to theory of mind in these disorders. Abu-Akel & Bailey
(2000) for example suggested
that there might be different forms of impairment of theory of mind. They
argue that, unlike people with autism-spectrum disorders, people with
schizophrenia do not lack an understanding that others have mental states;
instead, they may overattribute knowledge to others or apply their knowledge
of mental states in an incorrect or biased way. Thus, an interesting research
topic would be a comparison of the mentalising abilities of groups of people
with these two disorders.

Lastly, social impairment is one of the most disabling clinical features of
schizophrenia and it is well known that it is often present before illness
onset (e.g. Niemi et al,
2003). Since theory of mind impairment appears to be trait- rather
than state-dependent in schizophrenia, this deficit may have a role in the
development of social impairment. However, evidence of a relationship between
theory of mind performance and social functioning is lacking and should be an
aim of future research.

Acknowledgments

This study was supported by a grant from ZorgOnderzoek
Nederland/NWO-Medische Wetenschappen, project 2630.0001.

Sarfati, Y. & Hardy-Baylé, M. C.
(1999) How do people with schizophrenia explain the behaviour
of others? A study of theory of mind and its relationship to thought and
speech disorganization in schizophrenia. Psychological
Medicine, 29, 613
-620.